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Wednesday, June 27, 2012

Researchers at Columbia University in New York City have released a study showing a connection between a chemical commonly used in plastic household products and the risk that a young child will develop eczema. [press release] [paper] The work was widely covered in the media, including Fox News, which used a rather odd photo.

No, it's not BPA. It's benzylbutylphthalate (BBzP)--good luck pronouncing that--a component that seems to be found mostly in vinyl flooring, but which makes its way into dust, and thence into the body. However, the dominant source of BBzP is food, say the authors of the study, which was led by Allan Just at the Columbia Center for Children's Environmental Health.

BBzP is one of a class of compounds used to make plastics flexible. Scientists have little idea how it might interact with the skin and immune system.

For this study, the scientists took urine samples from pregnant women in the third trimester. Then, after the children were born, the mothers filled out questionnaires at regular intervals, noting whether their kids had had recurrent rashes or had a medical diagnosis of eczema.

The results, from a cohort of 407 women, showed that the chances of children developing eczema were positively correlated with the mother's prenatal BBzP concentration in the urine. The data makes it hard to give a simple number, but higher BBzP clearly means greater risk.

The pattern was similar for African-Americans and Dominicans, the two main ethnic groups represented in the study.

The scientists originally thought BBzP might increase the incidence or strength of allergies, but did not find that to be true in this work.

It's unclear what one can do about the issue, if the science is true. You don't have much control over your environment, especially if you live in an urban apartment, as virtually everyone does in NYC. And BBzP is only one of many factors, including genetics, gut flora, geographic location, diet, and parental smoking, thought to increase the risk of eczema.

Also, it seems that this problem, at least increasingly in the future, will be limited to the United States, since, as with BPA, Europe and Canada have recognized the toxic properties of BBzP and limited its use. The American Chemistry Council has most likely lobbied for BBzP’s continued use.

Tuesday, June 26, 2012

See my new post on the website of the National Eczema Association. It's about researchers at the University of Rochester who are conducting a clinical trial of Actos, a drug originally developed to treat diabetes but which looks like it could also repair the skin barrier and help eczema patients.

I learned about Actos when I spoke to Alice Pentland, who directs the new Skin Barrier Research Consortium at Rochester. I was going to write about the consortium but got too excited about Actos instead. I'll have to cover the research group in a second post.

Friday, June 15, 2012

The human microbiome was the star of this week's science news. In seventeen papers in the journals Nature and PLoS, the Human Microbiome Consortium published the genetic sequences for virtually all the microbes that live in or on the human body. I can't be alone in feeling overwhelmed by the volume of data and analysis. It's clear that the coming years will bring much research into how our body partners with, benefits from, and combats our microbial tenants--which outnumber our cells by a factor of ten.

In a Wall Street Journal story, Michael Fischbach, a professor at the University of California, San Francisco, was quoted as saying "It's likely this work will lead to new treatments for [the inflammatory bowel disorder] Crohn's disease, new treatments for diabetes and metabolic diseases, new treatments for even other diseases, like eczema."

Considering the various locations in the body, the gut and intestines contain the majority of microbes, as you can see in this graphic. A lot of recent work has shown connection between gut flora & systemic inflammation, particularly that involved in asthma and eczema.

A graduate student who reads this blog told me about one of these microbes: Helicobacter pylori. H. pylori has long lived in the human gut--until the twentieth century, it was apparently the most numerous microbe in the stomach. But it seems that antibiotics have since largely killed it off.

A lot of people would say this was a good thing: only about a decade ago, scientists discovered that H. pylori was the cause of stomach ulcers. But Martin Blaser, a prominent researcher at NYU who made a career out of studying H. pylori, has controversially claimed that it's not just a pathogen but can also do some good. Blaser says H. pylori used to protect us from developing allergic disease. The reason that allergic, atopic diseases are increasing in Western society, Blaser says, is that H. pylori isn't around any more.

The graduate student who wrote me gave me a link to a recent paper in which scientists prevent asthma from developing in lab mice by infecting newborn pups with H. pylori. They show that the way H. pylori is most likely working is that it stimulates the body to produce more regulatory T cells--a class of T cells that put a damper on the activity of other T cells.

In a 2008 story in the Economist, Blaser is portrayed as envisioning a future in which doctors colonize babies' digestive tracts with (presumably) non-pathogenic strains of H. pylori to protect the infants against atopic disease. Certainly a more aggressive form of probiotics than kimchi or yogurt! (Am I allowed to say "probiotics on steroids"?)

I could imagine, also, that there may be no need to use H. pylori at all. If you could arrange things so that a patient grew more Treg cells, that might have the same effect as a H. pylori infection, but a reduced risk of disease caused by the bacteria. Perhaps it will be possible to take a drug that increases the number of Treg cells. Or a patient could donate blood so that Treg cells could be extracted and grown in culture before being reinjected.

I'm excited about this area--admittedly only as speculation about what medicine may hold for us in the distant future. Whenever you're talking about altering the developing immune system, you have to be very careful. Of course, what do antihistamines and steroids do but alter the immune response?

Tuesday, June 12, 2012

You can generally separate eczema bloggers and tweeters into three groups. In increasing size of their representation on the web:

Those (e.g., me) who believe that Western science and medicine have good solutions to offer

People who believe that Western medicine is a conspiracy designed solely to funnel money into the pockets of big pharma (generally, wackos, although they may have a point)

Those who won't go as far as the second group, but who favor "natural" products and therapies instead of refined, "artificial' pharmaceuticals

I had an experience on the weekend that gave me a new look at the "natural" versus "artificial" debate. The idea that because something is part of a fresh or recently harvested plant (think Chinese herbs here) it's somehow kinder, softer, less likely to mess you up.

This is utterly wrong.

So, I found this cluster of healthy, clean-looking weeds outside my back gate. It looked like Italian parsley. It smelled like parsley. Did it taste like parsley? Whoa--let's not taste it right now, I thought.

And I'm a fan of wild mushrooms. I pick them and taste them raw. There is no mushroom that will kill you if you spit it out. Something just told me not to taste this plant.

I called my father-in-law, a biologist and naturalist, and he brought over a pile of books to help identify my weed. We narrowed it down to a few candidates that grow in our region.

Actual feral parsley

Water hemlock

Poison hemlock

Poison hemlock, according to our books, is the same herb the ancient Greeks used to kill Socrates. Next to the entry for poison hemlock, one of the books noted: "FATAL TO TASTE."

It also said that since so many plants in the parsley family are extremely poisonous, you shouldn't eat them unless you have absolutely, positively, identified them.

I don't know what this stuff is, but even though it's all-natural, I won't be using it to garnish my pasta.

And, by contrast, the same night I quite happily popped a few pills of ibuprofen to reduce my back pain. They worked just fine, like they always do. I don't mind paying big pharma for ibuprofen.

I know the comparison between poison hemlock and ibuprofen is hardly a fair one, and that most practitioners of Chinese medicine know what they're handling, but it did starkly illustrate the point that "natural" plants can produce some of the most evil toxins we know.

Friday, June 8, 2012

A moderate dose of ultraviolet light during the winter months increases the levels of vitamin D in the blood and appears to put a brake on the T-cell arm of the immune system--which could reduce the severity of autoimmune disease, a new small-scale study on a group of Scottish patients has shown.

The research was led by Mark Vickers and Anthony Ormerod, a professor and clinical reader in dermatology, respectively, at the University of Aberdeen. It was reported in the Journal of Allergy and Clinical Immunology.

The trial was conducted between December and March, 2012. Before and after exposing 24 subjects repeatedly to the equivalent of a quarter of a day's worth of summer sunlight, the scientists measured blood levels of vitamin D; the fraction of white blood cells comprised of "regulatory" T cells; and the degree to which T cells expanded their numbers when stimulated.

Regulatory T cells are a subset of T cells known to suppress the activity of other T cells. According to Wikipedia, "Mouse models have suggested that modulation of Tregs can treat autoimmune disease and cancer, and facilitate organ transplantation." Eczema with an allergic component qualifies as an autoimmune disease.

The scientists found that, after two weeks' exposure to UV, vitamin D levels increased by 50%; after four weeks, by 100%. The fraction of regulatory T cells increased threefold, and other classes of T cells reacted less vigorously to stimulation.

While I am always interested in the connection between vitamin D, T cells, and eczema--I wonder whether this study really tells us anything new. The American Academy of Dermatology says there is no safe recommended level of exposure to UV (because of the risk of skin cancer).
The connection between vitamin D and regulatory T cells appears to be well-established, according to a PubMed search I just did. And everyone knows that regulatory T cells suppress other T cells.

Having spent several years in the north of Scotland myself, I well know how little sunlight the Scots get in the winter. Were the subjects' vitamin D levels low to begin with? I bet they were. Could they benefit from supplements? Almost certainly.

Especially since, as I recall, the Scottish diet consists largely of chips, lager, and cigarettes!

Wednesday, June 6, 2012

The National Eczema Association has launched a blog on their website. I was honored to be asked to write the first post. "Well-moisturized infants less likely to develop eczema" is a summary of Eric Simpson and Hywel Williams' ongoing study of how moisturizing newborns provides them with barrier protection that can delay or maybe even prevent eczema from developing.

More posts are in the pipeline from other sources. The NEA expects that the blog will eventually feature the work of many different bloggers, including active scientists and clinicians as well as science writers. I look forward to discovering an ever-expanding community blogging eczema research, therapy, and coping strategies for parents and patients.

Something I've been meaning to cover is that Japanese scientists recently reported that they had developed a strain of lab mice in which the gene for filaggrin had been "knocked out."

That is, these mice, which are inbred for genetic purity, are missing the filaggrin gene. Their skin contains no filaggrin.

Filaggrin is a giant protein that consists of a chain of repeated components. It helps create the flattened structure of upper skin cells, and then breaks down into smaller, acidic molecules that form a natural moisturizing factor and probably help combat infection.

This will be a valuable experimental tool going forward. Paradoxically, a
mouse model without filaggrin can teach you a lot about what filaggrin
does--because it will be absent in those mice.

Using these new mice, researchers can focus on specific aspects of the skin, including various molecular pathways, and by comparing the knockout mice to regular mice, they can see what roles filaggrin plays.

Not surprisingly, the knockout mice have "dry, scaly skin" that lets more antigens through. Despite the skin's obvious fragility, the scientists find that the upper layers are normally hydrated, and show no increased tendency to lose water to the air.